Understanding How Alcohol Induces Human Acute Alcoholic Pancreatitis

Abstract

Why only a minority of heavy alcohol drinkers develop acute alcoholic pancreatitis has been a puzzle. In this review, the sparse data available from published studies were collected and, based on them, a hypothesis was formed. Long-term high alcohol consumption results in lowered cholecystokinin and cholinergic stimulus of the pancreas, and causes concentration and acidification of pancreatic fluid, predisposing to protein secretion. Early during the withdrawal period when returning to a normal or high-fat nonalcoholic diet, there is a relative hyperstimulation of the pancreas, a well-established mechanism that results in experimental acute pancreatitis. Lower, physiological stimulation is enough to start acute pancreatitis, when the secretions cause temporary obstruction in the duct system. The stimulation against temporary obstruction results in experimental acute pancreatitis. Finally, the magnitude of alcohol-induced deficits in acinar cell defense mechanisms determines the onset of pancreatitis.